Dual chamber pacing modes, particularly, the multi-programmable, DDD pacing mode, have been widely adopted for pacing therapy. This mode has a sensor augmented variant mode called "DDDR", where the "R" stands for rate-adaptive or rate modulation of the base or lower pacing rate as a function of a physiologic signal related to the need for cardiac output.
A DDD pacemaker includes an atrial sense amplifier to detect atrial depolarizations or P-waves, and a ventricular sense amplifier to detect ventricular depolarizations or R-waves. If the atrium of the heart fails to spontaneously beat within a predefined time interval (atrial escape interval), the pacemaker supplies an atrial pace pulse to the atrium through an appropriate lead system. Following an atrial event (either sensed or paced) and the expiration of an AV delay interval, the pacemaker supplies a ventricular pace pulse to the ventricle through an appropriate lead system, if the ventricle fails to depolarize on its own. Such AV synchronous pacemakers which perform this function have the capability of tracking the patient's natural sinus rhythm and preserving the hemodynamic contribution of the atrial contraction over a wide range of heart rates.
Many patients have an intact sinoatrial (SA) node that generates the atrial depolarizations detectable as P-waves, but inadequate AV conduction. For these patients, the DDD mode, which attempts to pace the ventricles in synchrony with the atria, is generally adequate for their needs. Patients with Sick Sinus Syndrome (SSS) have an atrial rate which can be sometimes appropriate, sometimes too fast, and sometimes too slow. For SSS patients, the DDDR mode provides some relief by pacing the atria and ventricles at a physiologic rate determined by a sensor which senses a physiological indicator of the patient's metabolic needs. DDDR pacemakers employing sensed cardiac impedance or pressure related parameters to derive a sensor related pacing rate include U.S. Pat. Nos. 4,566,456, 4,730,619, 4,899,751, 4,899,752, 4,936,304, 5,003,976, 5,163,429 and 5,330,511.
In DDDR pacing for SSS patients, reliance on the intrinsic atrial rate is preferred if it is appropriately within an upper rate limit and a lower rate limit. At times when the intrinsic atrial rate is inappropriately high or low, a variety of "mode switching" schemes for effecting switching between the DDD and DDDR modes (and a variety of transitional modes) based on the relationship between the atrial rate and the sensor derived pacing rate have been proposed as exemplified by commonly assigned U.S. Pat. No. 5,144,949, incorporated herein by reference.
Typically, the AV delay interval in such DDD and DDDR pacemakers is either fixed or varies with the prevailing spontaneous atrial rate, measured as an interval, or sensor derived atrial escape interval corresponding to the sensor derived atrial pacing rate. The variation of the AV delay as a function of the atrial escape interval in early AV synchronous pacemakers is disclosed, for example, in U.S. Pat. No. 4,108,148. The variation of the AV interval as a function of a sensed physiologic signal or an atrial escape interval pacing rate derived therefrom is disclosed in the above-referenced '511 patent and in U.S. Pat. Nos. 4,303,075 and 5,024,222.
The maintenance of AV mechanical synchrony is of vital importance in patients with compromised cardiac function, including hypertrophic cardiomyopathy, dilated cardiomyopathy, hypertensive heart disease, restrictive cardiomyopathy, congestive heart failure and other disorders that are characterized by significant diastolic dysfunction. In such patients, passive ventricular filling is reduced due to poor ventricular compliance and incomplete or delayed relaxation. Consequently, there is increased reliance on atrial contraction for ventricular filling sufficient to achieve adequate stroke volume and maintain low atrial and pulmonary pressure.
In addition, a loss of AV electrical and mechanical synchrony can result in series of asynchronous atrial and ventricular depolarizations at independent rates that periodically result in an atrial depolarization that closely follows a ventricular depolarization. When this occurs, the left atrium contracts against a closed mitral valve, resulting in impeded venous return from the pulmonary vasculature due to increased atrial pressure and possibly even retrograde blood flow into the pulmonary venous circulation. As a result, the volume and pressure in the pulmonary venous circulation rise. Increased pulmonary pressures may lead to pulmonary congestion and dyspnea. Distention of the pulmonary vasculature may be associated with peripheral vasodilation and hypotension. In addition, the concomitant atrial distention is associated with increased production of atrial natriuretic factor and increases the susceptibility to atrial arrhythmias and possibly rupture of the atrial wall. Finally, turbulence and stagnation of blood within the atrium increase the risk of thrombus formation and subsequent arterial embolization. Restoration of AV mechanical synchrony would be expected to reverse these deficits.
Theoretically, AV synchrony is maintained during dual chamber cardiac pacing by setting the AV delay interval in a physiological range related to the spontaneous atrial rate or the sensor derived rate, depending on which is the controlling pacing mode, as described above. However, while "physiological" AV delays may ensure right heart AV electrical synchrony, in patients with significant interatrial and/or interventricular conduction delays, left heart electrical and mechanical synchrony, and thus hemodynamic performance, may be significantly compromised. The monitoring of left heart AV mechanical synchrony during pacemaker programming could aid in establishing the optimal pacemaker AV delay for peak hemodynamic performance. Likewise, incorporation of such monitoring capability into a pacemaker device could permit continuous adjustment of the pacemaker AV delay to maintain optimal left heart AV mechanical synchrony and function. However, due to the high left heart pressure and the risk of tamponade and thromboembolism, pacing leads and sensor probes cannot readily be placed in or on the left heart.
Under steady state conditions, a loss of left heart AV mechanical synchrony may be expected to produce an increase in pulmonary capillary wedge pressure and pulmonary artery systolic and diastolic pressure. Therefore, a sensor capable of detecting such changes could be used as a monitor for steady state changes in left heart AV mechanical synchrony. Initial feasibility studies have been performed in which pulmonary vascular pressure was monitored by a sensor lead chronically positioned in the pulmonary artery as described by Steinhaus et at., in "Initial Experience with an Implantable Hemodynamic Monitor" Circulation, vol. 93, no. 4, Feb., 1996, pp. 745-52. More recently, it has been reported that a right ventricular absolute pressure sensor, being developed by the assignee of the present invention, can be used to derive an estimated Pulmonary Artery Diastolic (EPAD) and pulmonary capillary wedge pressure as described by Ohlsson et al, in "Monitoring of Pulmonary Arterial Diastolic Pressure Through a Right Ventricular Pressure Transducer", Journal of Cardiac Failure, vol. 1, no. 2, 1995, pp. 161-168 and by Reynolds et al., in "Measurement of Pulmonary Artery Diastolic Pressure From the Right Ventricle", JACC, vol. 25, no. 5, Apr., 1995; 1176-82. An implantable system for providing such monitoring is disclosed in commonly assigned U.S. Pat. No. 5,368,040. An absolute pressure sensor and circuitry for developing an absolute right ventricular or other heart chamber or vessel pressure signal is described in detail in commonly assigned U.S. patent application Ser. No. 08/394,870 filed Feb. 2, 1996, for IMPLANTABLE CAPACITIVE ABSOLUTE PRESSURE AND TEMPERATURE SENSOR and Ser. No. 08/394,860 filed Feb. 2, 1996, for IMPLANTABLE CAPACITIVE ABSOLUTE PRESSURE AND TEMPERATURE MONITORING SYSTEM.